STAMI- Stunning in Takotsubo Versus Acute Myocardial Infarction

Prospective assessment of the temporal electrocardiographic-, vectorcardiographic- and echocardiographic changes in STelevation myocardial infarction versus the takotsubo syndrome.

AIM To compare the temporal pattern of myocardial funtional recovery after ST-elevation myocardial infarction (STEMI) versus the takotsubo syndrome (TS).

BACKGROUND Modern therapies have reduced the incidence of acute ischemic heart failure (AIHF) -But AIHF is still common and once it develops prognosis remains dismal.Despite considerable therapeutic advancements over the last decades, acute myocardialinfarction (AMI) remains one of the most common causes of death . Among patients who are admitted with AMI, the 10% that develop AIHF account for approximately 50% of Deaths within 30 days . The prognosis for patients with AIHF has not improved over the last decade . AIHF occurs due to acute loss of cardiac function, some of which occurs in myocardium that is not irreparably damaged - so called stunned myocardium.

Myocardial stunning in AIHF - Temporary mechanical dysfunction without irreparable injury. Myocardial stunning was originally described in the setting of ischemia and was defined as temporary mechanical dysfunction that persists after resolution of ischemia, with the absence of irreversible histological damage . For the purpose of this application it is more broadly defined as temporary mechanical dysfunction, with the absence of irreversible histological damage - irrespective of the underlying cause. Myocardial stunning is believed to be a harmful phenomenon caused by cellular injury .

Study hypothesis: Myocardial stunning is a protective mechanism by which the cardiomyocytes preserve energy for vital processes in states of severe cellular stress - but that can "overshoot" and lead to potentially lethal cardiac decompensation. In the normal heart, the contractile apparatus consumes the majority of myocardial energy and oxygen . Non-contractile myocardial functions, including cellular and electrical homeostasis, require less than 20% as much oxygen. When oxygen supply to the heart is interrupted myocardial stunning ensues within seconds, whereas it takes at least 10 minutes for the cardiomyocyte's energy metabolites to decrease to 50% of their initial level .Hence, by shutting down the contractile apparatus before it consumes the cells' energy stores myocardial stunning effectively preserves energy for processes that are necessary for cell survival . Irrespective of its beneficial effects on cardiomyocyte metabolism, myocardial stunning may lead to sufficiently pronounced cardiac dysfunction to cause life-threatening AIHF.